AIM: To investigate the relation between the changes of the cerebral microvasculature and the expression of plasminogen activator inhibitor-1 (PAI-1) in ischemic focal and perifocal areas after 2 hours focal cerebral ischemia with reperfusion in rats. METHODS: The changes of cerebral microvascular structure were observed by optical microscope and electric microscope, the expression of PAI-1 were assessed by immunohistochemical staining, Western blotting in ischemic focus and perifocal areas after focal cerebral ischemia with reperfusion. RESULTS: The edema of extra-cellular matrix and the hemorrhage of extravessels in ischemic focus and perifocal areas were most severe, and degradation and the defect of basement membrane were also observed after 6 hours and 3 days reperfusion following focal cerebral ischemia. The expression of PAI-1 decreased significantly compared with control group (P

AIM: To explore clinical significance of the serum changes of neuron-specific enolase (NSE)and S-100 ? protein (S-100 ?) during acute cerebral infarction. METHODS: 59 acute cerebral infarction patients were classified as total anterior circulation infarcts (TACI), partial anterior circulation infarcts (PACI), lacunar infarcts (LACI) and posterior circulation infarcts (POCI). Their serum NSE and S-100 ? concentrations were determinated by enzyme linked immunosorbent assay (ELISA) during stroke onset 6 d, and compared with 32 controls. RESULTS: The every time point serum NSE concentration of TACI was higher than controls (P

Objective 　To search the relative factors of cerebral damage, rebleeding, delayed cerebral ischaemia(DCI) and hydrocephalus after subarachnoid haemorrhage (SAH) by CT scans and clinical findings in acute phase. Methods　To analyse the relationship between cerebral damage after SAH and clinical findings: CT scans resulte, age, sex, blood pressure, hyponatraemia, therapeutic methods. Results　Cerebral damage were related to the pattern of distritution of SAH on brain CT and hyponatraemia. The high attack rate of rebleeding and DCI is related to presence of blood in the surface of brain, collection of blood in the ventricle, saccula aneurysms or cerebral arteriovenous malformation (AVM) (P＜0.01). Conclusions　To forecast of cerebral damage after SAH by study of CT scans showing and clinical findings have clincal significance. According to these findings, we may take some therapeutics to prevent the cerebral damage after SAH.

AIM: To explore the structural changes of brain microvasculature and mechanism in microvascular lesion after focal cerebral ischemia with reperfusion. METHODS: Using the techniques of immunohistochemical staining, in situ hybridization,optical microscopy and transmission electron microscopy, the expression of uPA, uPA mRNA, and changes in miocrovascular structure were examined in ischemic focus and perifocal areas after focal cerebral ischemia 2 hours with various time points of reperfusion in stroke-prone renovascular hypertensive rats (RHRSP). RESULTS: The brain edema and hemorrhage were severe 12 hours to 3 days after reperfusion. Ultrastructural change showed that the damage characterizations of the basement membrane were degradation, defection, and exfoliated of basement membrane, while uPA, which attack the basememt membrane around cerebral capillaries and extra-cellular matrix, and uPA mRNA expression increased significantly in ischemic and perifocal areas 12 hour to 3 day after reperfusion. CONCLUSION: The main pathologic mechanism of brain edema and hemorrhage after cerebral ischemia with reperfusion may result from the basement membrane lesion of brain microvasculature. The increase in the expression of uPA in reperfusion area may be the main cause of the basement membrane lesion .

ObjectiveTo verify the reliability of the mouse model of cerebral cortical microinfarct induced by two-photon microscopy and to explore its pathological changes.MethodsSeventeen male C57BL/6J mice were randomly divided into a microinfarct group (n=11) or a sham operation group (n=6).A thinned cranial window of 3 mm diameter was performed over the cerebral cortex with a high-speed micro-drill until the small blood vessels were clearly observed under a dissecting microscope.Then, a permanent single cortical penetrating arteriole occlusion was induced with a gradually enhanced ultrashort laser irradiation through the thinned cranial window with two-photon microscopy.At 7 days after modeling, the cerebral microinfarct volume was measured with HE staining, and the neuron loss, activation of glial cells and deposition of 3-nitrotyrosine were assessed using immunohistochemistry.ResultsThe target vessels of cerebral cortex in 8 (72.7%) mice were occluded and the microinfarcts formed in the microinfarct group, and the average microinfarct volume was 317.23±20.29 μm3.There were remarkable neuron loss and microglia infiltration in the infarcted core, a large number of reactive astrocytes surrounding the infarcted lesion, and massive deposition of 3-nitrotyrosine in the peri-infarct area.No infarcts were observed in the sham operation group.The deposition of 3-nitrotyrosine in the sham operation group was significantly less than that in the microinfarct group (8.00±1.48 vs.98.38±9.10;t=23.962, P<0.001).Conclusions The mouse model of cerebral cortical microinfarct induced by two-photon microscopy is reliable, and its histopathologic changes are consistent with the pathologic features of cerebral microinfarct.

ObjectiveTo explore the effects of the serum of traditional Chinese medicine Nao Yi An on glutamate induced cell death in cultured hippocampal neurons of rat and the underlying mechanisms. MethodsHippocampal neurons were cultured. The excitatory amino acid induced toxicity on cultured neurons was investigated. The viability of injured neurons was determined with the measurement of Lactate dehydrogenase (LDH) activity. Mitogen activated protein kinase (MAPK) were determined by immunoprecipitation /kinase assays /western blot detection.ResultsThe serum of Nao Yi-An raised cell viability. The serum of Nao Yi-An upregulated the expression of extracellular regulated protein kinases(ERK) and downregulated the expression of c-Jun N terminal kinase/stress activited protein kinase(JNK) in cultured neurons. The serum of Nao Yi-An induced upregulation of ERK and its anti death action were prevented with the specific ERKs inhibitor PD98059. Conclusions Activation of ERK signaling together with inhibition of JNK signaling by Chinese medicine Nao Yi-An appears to be an important mechanism for its survival effects on cultured hippocampal neurons.

Objective Evaluation of cerebral blood flow in patients with transient ischemic attack (TIA) using cerebral CT perfusion imaging.Methods CT perfusion scan was performed on a consecutive series of 20 patients with clinical definite TIA.Following their initial CT scan at acute stage of TIA, patients underwent two repeat CT perfusion scanning of region of interest at acute stage and one month after symptom remission.Results Mild to moderate decrease in regional cerebral blood flow (rCBF) and unchanged or mildly decrease in regional cerebral blood volume (rCBV) were observed at acute stage in the majority cases.Normal cerebral perfusion was found in 12 cases and mild to moderate decrease of rCBF in 8 cases one month after TIA.During the one-year follow-up period, all of 12 cases with normal cerebral perfusion did not have recurrence while among 8 cases with mild to moderate decrease of rCBF at initial scan, 6 cases had recurrent TIA or cerebral infarction and 2 cases did not have recurrence.Patients with more severe cerebral perfusion defects usually had a shorter interval time between two attacks.Conclusions Intensive intervention should be performed on patients with severe and long lasting decrease of cerebral perfusion.

Objective To investigate the correlation between the measurement methods of carotidcerebral pulse wave velocity (ccPWV) and the traditional method of brachial-ankle pulse wave velocity (baPWV).Methods A total of 136 healthy volunteers were divided into a youth group (20-39 years),a middleaged group (40-59 years),and an elderly group (more than 60 years) according to their ages.While detecting baPWV,transcranial Doppler ultrasound was used to simultaneously monitor the ipsilateral common carotid artery and the terminal segment of internal carotid artery.The time differences of the beating points of their cardiac cycles and the distanceses of the skin surfaces between the 2 probes were measured and ccPWV was calculated.Results The systolic blood pressure,pulse pressure and mean arterial pressure in the elderly group were signifificantly higher than those in the middle-aged group and the young group.The ccPWVs in the youth,middle-aged and elderly groups were 418 ± 52 cm/s,489 ±54 cm/s,and 599 ± 58 cm/s,respectively.The elderly group was significantly faster than the middle-aged group (t =7.308,P ＜0.001),and the middle-aged group was significantly faster than the youth group (t=6.758,P＜0.001).A Pearson correlation analysis showed that ccPWV was significantly positively associated with the age (r=0.847,P＜0.001) and baPWV (r =0.548,P ＜0.001).The multiple linear regression analysis showed that ccPWV was significantly positively associated with the age and diastolic blood pressure (partial correlation coefficients were 0.742 and 0.293respectively,P ＜0.001 and ＜0.010 respectively).Conchlusions ccPWV is a new measurement method for cerebrovascular stiffneas,and it has a good correlation with the traditional measurement method.

Objective To investigate the preventive effect and mechanisms of Naoshuantong capsule in stroke induced by artificial cold wave in hypertensive rats.Methods A total of 130 SD rats were randomly divided into a sham operation group (n =30),a model control group (n =50) and a Naoshuantong treatment group (n=50;intragastric administration of Naoshuantong,0.5 g/kg,2/d for 7 days).Renovascular hypertensive rats model were established by two-kidney,two clip method.At 13th week after operation,rats were exposed to artificial cold wave for 3 days (12 h light of 22 ℃ and 12 h dark of 4 ℃,3 cycles).The brain tissue samples were extracted at the end of the experiment.Differential protein proteomic techniques were used for the identification,functional classification and preliminary analysis of the differentially expressed protein spots,and Western blot was used for the validation of some key proteins.Results There was no occurrence of stroke in the sham operation group,and the incidence of stroke in the model control group (36.00％,18/50) was significantly higher than that in the Naoshuantong treatment group (18.00％,9 / 50;x2 =4.110,P =0.043).With the two-dimensional gel electrophoresis analysis,6 different proteins were identified from 14 protein spots.Among them,the up-regulated superoxide dismutase 2 (SOD2) and the down-regulated B-cell lymphoma 10 (Bcl-10) were found to be at the central location of protein interactions,which has been verified by Western blot.Conclusion Naoshuantong can reduce the occurrence of stroke induced by artificial cold wave in renovascular hypertensive rats.SOD2 up-regulating and Bcl-10 downregulating may be involved in the mechanisms of of Naoshuantong in the prevention of cold wave-induced stroke in hypertensive rats.

Epidemiological studies and clinical observations have indicated that cold temperature can trigger the occurrence of stroke in individuals at high risk.However,the underlying mechanisms are still unknown.Matrix metalloproteinase-9 (MMP-9) has been found to be associated with the formation,progression and rapture of atherosclerotic plaques and cerebral aneurysms,which is the pathological basis of stroke.Cold temperature activates renin-angiotensin system (RAS) in circulation and tissue.Angiotensin Ⅱ has been implicated in the inducing MMP-9 expression and activation.An increase of MMP-9 may facilitate destabilization and rupture of atherosclerotic plaques or cerebral aneurysms,resulting in the occurrence of stroke.